【摘 要】
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The tumor suppressorphosphatase and tensin homolog deleted on chromosome 10 (PTEN) is frequently mutated or deleted in many types of tumors.PTEN germline mutati
【机 构】
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Department of Radiation Oncology, The Cancer Institute of New Jersey, University of Medicine and Den
论文部分内容阅读
The tumor suppressorphosphatase and tensin homolog deleted on chromosome 10 (PTEN) is frequently mutated or deleted in many types of tumors.PTEN germline mutations have been found in several familial cancer predisposition syndromes such as Cowden syndrome,Lhermitte-Duclos disease,Bannayan-Riley-Ruvalcaba syndrome and Proteus and Proteus-like syndromes.As a lipid phosphatase,PTEN dephosphorylates phosphatidylinositol 3,4,5-trisphosphate (PIP3),the second messenger produced by phosphatidylinositol 3-kinase (PI3K),and therefore negatively regulates the PI3K/AKT signaling pathway.The PI3K/AKT pathway plays a critical role in driving cell proliferation and cell survival,which is frequently activated in tumors and contributes to tumorigenesis.Loss of PTEN leads to the accumulation of PIP3,which in tu recruits phosphatidylinositol-dependent kinase 1 (PDK1) and AKT to plasma membrane where PDK1 phosphorylates and activates AKT.By negative regulation of the oncogenic PI3K/AKT pathway,PTEN functions as a tumor suppressor.
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